It is known that the definition of the term tumor necrosis factor (TNF) includes two cytotoxic factors (TNF- .alpha. and TNF-.beta.) which are essentially formed by activated lymphocytes and monocytes. The term TNF derives from the property which initially attracted particular attention from those skilled in the art: TNF has a necrotic effect on certain tumors in vivo. This effect was found for the first time when it was observed that, in cases of cancer, bacterial infections may result in a regression of the tumor. It was initially assumed that lipopolysaccharides from the cell walls of bacteria, which are called endotoxin, are responsible for the regression of the tumor. However, it was later shown that the endotoxin itself had no direct antitumor effect but in turn induces the formation of a factor which is responsible for the tumor necrosis. This factor was then called TNF. Further investigations later revealed that TNF is principally formed by macrophages. It was likewise shown, by stimulation of lymphocytes in vitro, that there is formation of a substance having cytotoxic activity, which was called lymphotoxin. The close relationship between TNF and lymphotoxin was only recently discovered after the two proteins had been prepared in pure form, their primary structure had been established and their cDNAs had been isolated and expressed. This revealed remarkable similarities in the two proteins and their genes. Great similarities were also evident from the biological activities of these two proteins. For this reason, they were called TNF-.alpha. and TNF-.beta., corresponding to their formation from monocytes or lymphocytes.
Once relatively large amounts of TNF became available by application of methods of genetic manipulation for the preparation, it emerged that, besides its antitumor effect, TNF also has a large number of other effects. They are described in detail by Bharat B. Aggarwal in "Drugs of the Future" 12 (1987), pages 891 et seq. Overall, it has to be stated that TNF carries out an important task in the immune system of the body but that there may be overproduction of TNF in certain infections, diseases or injuries, and this may be life-threatening. For this reason, there has also already been a proposal that a TNF inhibitor be used in certain pathological states where there is overproduction of TNF. Monoclonal antibodies directed against TNF have already been proposed for this purpose (Nature, vol. 330, pages 662 et seq.). Moreover, it has already been disclosed that shock induced by endotoxin can be prevented by previous administration of pentoxifylline (Clinical Hemorheology, vol. 6, 1986, pages 455-467).